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Biomedical subjects

J Mehta

Publications and source records attributed to J Mehta.

At least 379 records · Page 21Linked to original sources
PubMedDate not supplied

Effect of altered lymphocyte function on immunologic disorders in NZB/NZW mice.

NZB/NZW F1 female mice were treated with the immunosuppresive enzyme L-asparaginar antibodies, diminished deposition of gamma-globulins in kidneys, significantly delayed the onset of proteinuria, and reduced deaths from nephritis. These effects were associated with reduction of cellular IgM antibody synthesis to both T-dependent and T-independent antigens, but the graft-versus-host reaction was not affected. After several weeks of therapy, antibodies against Asnase appeared in the circulation, the effect on antibody synthesis was lost, ANA and anti-DNA appeared, followed by proteinuria and deaths from nephritis. Therefore Asnase proved to be an effective therapy in NZB/NZW mice, but its usefulness was limited by the appearance of inactivating antibodies.

Animals↗
PubMedDate not supplied

Potentiation of endoperoxide analog-induced platelet aggregation by heparin.

The mechanism of heparin-induced platelet aggregation potentiation is much debated. We examined the effects of heparin on platelet aggregation induced by cyclic endoperoxide analog u46, 619. Heparin enhanced platelet aggregation in a dose-related fashion. Potentiation of platelet aggregation was also found to be related to the incubation time of heparin and platelet rich plasma. Porcine intestinal heparin and bovine lung heparin exhibited similar patterns. To test the hypothesis of increased platelet thromboxane A2 production under the influence of heparin, we measured U46,619-induced thromboxane A2 generation. Heparin was found not to affect platelet thromboxane A2 generation over a wide range of concentrations. The platelet aggregation potentiating actions of heparin are thus unrelated to thromboxane A2 pathway.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMedDate not supplied

Failure of cyclosporine to induce graft-vs-host disease or graft-vs-leukemia after syngeneic bone marrow transplantation in mice.

Cyclosporine administration can result in graft-vs-host disease (GVHD) after syngeneic or autologous bone marrow transplantation (BMT). However, data on its anti-tumor effects are limited. We have tried to produce cyclosporine-induced GVHD or graft-vs-leukemia (GVL) against two Ia-bearing murine leukemias. BALB/c mice undergoing syngeneic BMT after total-body irradiation received 1 mg/kg or 10 mg/kg cyclosporine or dextrose intraperitoneally for 30 days post-transplant, followed by 5 x 10(3) BCL1 murine leukemia cells 1 or 3 weeks after stopping cyclosporine. Similarly, SJL/J mice undergoing syngeneic BMT received 10 mg/kg cyclosporine or dextrose intraperitoneally for 30 days post-transplant, and were inoculated with 5 x 10(3) or 10(5) murine acute myeloid leukemia (mAML) cells 3 weeks after stopping cyclosporine. No clinical or histological evidence of GVHD was seen, and leukemia-free and overall survival was similar with cyclosporine and dextrose. We conclude that under the experimental conditions used, it is not possible to induce syngeneic GVHD with cyclosporine in BALB/c or SJL/J mice. In the absence of GVHD, this approach is also not associated with any GVL effect against murine leukemias BCL1 and mAML.

Animals↗
PubMedDate not supplied

Fluorimetric method for the detection of anti-DNA antibodies in serum.

A method for the detection of native anti-DNA antibodies in serum is described. The method is based on the reactivity of fluorescein isothiocyanate with DNA, forming a complex capable of combining with anti-DNA antibodies. The fluorescein content of the precipitated fluorescein-DNA anti-DNA complex is then measured in a fluorometer. The assay is accurate, highly reproducible, and inexpensive to perform. Comparative studies performed with the Farr assay show the fluorimetric method to be more sensitive in detecting anti-DNA antibodies in the serum of SLE patients.

Antibodies, Antinuclear↗
PubMedDate not supplied

Dipyridamole and aspirin in relation to platelet aggregation and vessel wall prostaglandin generation.

Modification of platelet function and vessel wall prostaglandin synthesis by pharmacologic intervention has attracted considerable attention. We report our observations on the effects of aspirin and dipyridamole alone and their combination on platelet aggregation and vessel wall prostacyclin (PGI2) generation. Although dipyridamole alone had no effects on platelet aggregation, it potentiated the platelet aggregation inhibitory effects of aspirin in vitro in a dose-related fashion. Dipyridamole also enhanced the platelet aggregation inhibitory effect of synthetic PGI2 in vitro. Potentiation of aspirin- and PGI2-induced platelet aggregation inhibition was observed in therapeutic range (5-10 micrograms/ml). In an isolated umbilical vein model dipyridamole stimulated release of PGI2 at much higher concentration (50-100 microgram/ml). Treatment of umbilical vein with aspirin (180 micrograms/ml) for 10 min blocked the spontaneous release of PGI2. In aspirin-treated umbilical vein segments dipyridamole treatment did not cause PGI2 release as in the untreated segments. These experiments suggest that although dipyridamole enhances both aspirin- and PGI2-induced platelet aggregation inhibition in clinically achieved concentrations, much higher levels are necessary for PGI2 release from intact human vessels. Furthermore, aspirin treatment of human vessels may prevent release of PGI2 in response to dipyridamole by blocking cyclooxygenase enzyme.

6-Ketoprostaglandin F1 alpha↗
PubMedDate not supplied

Antioxidants and vitamins in your cardiac patient: are they helpful?

There is an intense interest in the use of antioxidants in the prevention and treatment of coronary artery disease (CAD). Oxidants or free radicals are necessary for human physiology, but excess of free radical formation and release can lead to vascular injury and lipid peroxidation. Some, but not all, studies show beneficial effect of exogenous antioxidants, primarily vitamin E, in patients with CAD. This article summarizes our current understanding of free radicals and their role in physiology and the role of antioxidants in disease prevention with special emphasis on the potential adverse effect of treatment of patients with large doses of antioxidants.

Antioxidants↗
PubMedDate not supplied

Circulating platelet aggregates in sickle cell disease patients with and without vaso-occlusion.

In vivo circulating platelet aggregates (CPA) were evaluated in 18 patients aged 6 to 17 years with sickle cell disease and in 11 age and sex matched normal subjects. Twelve patients with sickle cell disease were in steady state and 6 had vaso-occlusive crises. CPA in patients in steady state were similar to those in normal subjects (mean 6 +/- 1% compared to 5 +/- 2%, respectively), whereas patients with vaso-occlusive crisis in acute state had significantly higher CPA (mean 39 +/- 8%) than patients in steady state or normal control individuals (both p less than 0.001). CPA decreased in patients with vaso-occlusive crisis (mean 11 +/- 4%) on the tenth day, in association with clinical improvement. This study suggests that in vivo platelet aggregate formation activity, although normal in sickle cell disease patients in steady state, is significantly increased in patients with vaso-occlusive crises.

Adolescent↗
PubMedDate not supplied

Effect of clofazimine and dapsone on rifampicin (Lositril) pharmacokinetics in multibacillary and paucibacillary leprosy cases.

A comparative pharmacokinetic study of Lositril (rifampicin) was carried out in six multibacillary and twelve paucibacillary leprosy cases. The type of leprosy had no significant effect on rifampicin pharmacokinetics. The effect of dapsone and clofazimine when given separately and in combination was studied on rifampicin pharmacokinetics in each group of six patients. Within group comparison revealed that clofazimine reduced rifampicin absorption significantly (P less than 0.01) and prolonged the time to reach the peak serum concentration (P less than 0.01). Since MCR and Ke were also reduced significantly in RC group, as compared with RDC group (P less than 0.02 and P less than 0.05 respectively), no significant alteration was seen in overall Auc and Cmax, although t0.05 was increased significantly (P less than 0.02) in RC Group. Dapsone alone did not produce any significant alteration in rifampicin pharmacokinetics parameters, while dapsone with clofazimine reduced rifampicin 1h serum levels (P less than 0.05) and Auc (P less than 0.05) significantly. Of the three groups, except RC group, both RDC and RD groups were homogeneous Ka, avd, Cmax and Auc/t0.5 ratio of RC group were significantly different from those in RD group. While Ka and avd were significantly less (P less than 0.05 and less than 0.001 respectively) and Cmax and Auc/t0.5 ratio were significantly more (P less than 0.01) in RC group. Since clofazimine reduced rifampicin absorption, the difference in Ka and tp became more significant in the post-regimen phase (P less than 0.01).

Adolescent↗